Dentine hypersensitivity is a common but painful condition affecting 18-42% of the adult population and has been defined as “short, sharp pain arising from exposed dentine in response to stimuli, typically thermal, cold, evaporative, tactile, osmotic or chemical which cannot be ascribed to any other form of dental defect or pathology” (Int. Dent. J. 2002; 52: 367-375). The primary origin is generally agreed to result from the exposure of dentine following either loss of the protective enamel layer or via gum recession.
The most pronounced morphological characteristic of human dentine is its tubular structure. Dentine tubules have diameters in the order of several micrometers and connect the pulp to the enamel dentine junction. In a healthy subject, these tubules are filled with fluid. It is postulated that this dental fluid plays an active role in the transmission of pain stimuli across the dentine to the underlying neurons. This widely-accepted theory, known as the hydrodynamic theory, states that when the dentine tubules become exposed to the environment, external stimuli elicit a displacement of the dentinal fluid, which, in turn, stimulates mechanoreceptors in the pulp. The movement of fluid through the narrow tubules irritates cells in the vicinity of the base of the tubules, including odontoblasts, pulpal neurons, and even subdontoblastic blood vessels. Several researchers have shown that the fluid movements result in the release, from the pulpal nerves, of calcitonin gene-related peptide, which generates a local neurogenic inflammatory condition.
There are two categories of therapy for the treatment of dentine hypersensitivity based upon two modes of action. The first category, nerve-depolarising agents, are pharmaceutical agents such as potassium nitrate which function by interfering with neural transduction of the pain stimulus.
The second category, known as occluding agents, function by physically blocking the exposed ends of the dentinal tubules, thereby reducing dentinal fluid movement and reducing the irritation associated with the shear stress described by the hydrodynamic theory.
The occlusion approach typically involves treating the tooth with a chemical or physical agent that creates a deposition layer within or over the dentine tubules. This layer mechanically occludes the tubules and prevents or limits fluid movement within the tubule to such an extent that stimulation of the neuron is not achieved. Examples of occlusion actives include among others, calcium salts, oxalate salts, stannous salts, glasses, inorganic oxide particles e.g. SiO2, Al2O3 and TiO2 and polymers e.g. methylmethacrylate based varnishes.
U.S. Pat. No. 5,270,031 (Block) relates to water soluble or water swellable polymers with functional groups that are capable of bearing one or more charged groups in an aqueous solution having desensitising properties. Such polymers can be anionic, cationic or amphoteric. One example of an anionic functional group is the carboxylate group which is found in polymers such as polyacrylic acid, copolymers of acrylic acid and maleic acid, copolymers of methacrylic acid and acrylic acid, and copolymers of alkyl vinyl ethers and maleic acid or anhydride.
U.S. Pat. No. 5,885,551 (Block) relates to a method of treating dentinal hypersensitivity by administering alginic acid or an alginate in an oral care composition.
U.S. Pat. No. 6,096,292 (Block) relates to the use of a superabsorbent acrylic polymer as a desensitising agent.
U.S. Pat. No. 6,241,972 (Block) relates to compositions and their use in treating dentinal hypersensitivity comprising a copolymer having repeated units of a hydrophilic monomer such as a carboxylic acid, a dicarboxylic acid or a dicarboxylic acid anhydride and a hydrophobic monomer consisting of an alpha-olefin having at least eight carbon atoms, full and partially hydrolysed forms thereof and full and partial salts thereof.
Despite the above proposals, there remains a need for alternative treatments for alleviating dentine hypersensitivity.